Abnormal increase in blood uric acid level, i.e., hyperuricemia is a disease which closely relates to gout, renal dysfunction, urolithiasis, and the like (Shindan to Chiryo, 2002, 90(2), 244-248 and Shindan to Chiryo, 2002, 90(2), 220-224). Also, in organ transplantation (Ren. Fail. May 2002; 24(3): 361-7) and chemotherapy of cancers (Am. J. Health Syst. Pharm. Nov. 1, 2003; 60(21): 2213-22), it is known that serum uric acid level is remarkably increased and renal dysfunction is induced (tumor lysis syndrome and the like). The therapeutic drugs for hyperuricemia are roughly divided into uric acid-excretion accelerators and uric acid-synthesis inhibitors. However, since the action is reduced in the uric acid-excretion accelerators when renal function decreases, allopurinol (Nippon Rinsho, December 1996; 54(12): 3364-8 and Nippon Rinsho, 2003; 61, Suppl. 1: 197-20) which is a uric acid-synthesis inhibitor is suitably used for patients having decreased renal function (Guideline for therapy of hyperuricemia/gout, Japanese Society of Gout and Nucleic Acid Metabolism, Therapeutic Guideline 2002). Xanthine oxidase is an enzyme directing biosynthesis of uric acid, and xanthine oxidase inhibitors which inhibit the enzyme is effective, as uric acid-synthesis inhibitors, for therapy of hyperuricemia and various diseases attributable thereto. Allopurinol employed in clinical use is only one xanthine oxidase inhibitor which is in practical use, at present.
On the other hand, xanthine oxidase is known to have a role as an active oxygen-producing enzyme (Drug Metab. Rev. May 2004; 36(2): 363-75). Active oxygen is a exacerbation factor of morbid conditions, which causes DNA and cell damage and also induces inflammatory cytokine production (Free Radic. Biol. Med. May 15, 2001; 30(10): 1055-66). For example, it is known that active oxygen deeply participates in autoimmune and inflammatory diseases such as ulcerative colitis and Crohn's disease (Scand. J. Gastroenterol. December 2001; 36(12): 1289-94) and ischemic reperfusion disorder (Biochem. Biophys. Res. Commun. Mar. 5, 2004; 315(2): 455-62). Furthermore, recently, in diabetic kidney diseases (Curr. Med. Res. Opin. March 2004; 20(3): 369-79), heart failure (J. Physiol. Mar. 16, 2004; 555(Pt 3): 589-606, Epub 2003 Dex 23), cerebrovascular disorder (Stroke, April 1989; 20(4): 488-94), and the like, it is suggested that active oxygen participates in as one of exacerbation factors. Moreover, in diabetic retinopathy, it is known that an increase in vascular endothelial growth factor (VEGF) in the vitreous body deeply participates in morbid condition and an increase in expression of VEGF through oxidation stress occurs under morbid conditions (Curr Drug Targets. June 2005; 6(4): 511-24). Since a xanthine oxidase inhibitor inhibits production of active oxygen, it is effective in treatment of these diseases. Actually, it has been reported that allopurinol is effective in ulcerative colitis (Aliment. Pharmacol. Ther. September 2000; 14(9): 1159-62), angiopathy involved in diabetes (Hypertension, March 2000; 35(3): 746-51), and chronic heart failure (Circulation, Jul. 9, 2002; 106(2): 221-6) in human.
As above, although allopurinol which is a xanthine oxidase inhibitor is reported to have effectiveness for various diseases, severe adverse effects such as Stevens-Johnson syndrome, toxic epidermal necrolysis, hepatopathy, and renal dysfunction have been reported (Nippon Rinsho, 2003; 61, Suppl. 1: 197-201). As one cause thereof, it is pointed out that allopurinol has a nucleic acid-like structure and inhibits pyrimidine metabolic pathway (Life Sci. Apr. 14, 2000; 66(21): 2051-70). Accordingly, it is highly desired to develop a highly safe and highly effective xanthine oxidase inhibitor having a non-nucleic acid structure.
Hitherto, compounds having xanthine oxidase-inhibitory activity have been reported. For example, as xanthine oxidase inhibitors, there have been reported phenyl-substituted azole compounds such as 2-phenylthiazole derivatives (Patent Documents 1, 2, and 3), 3-phenylisothiazole derivatives (Patent Documents 4 and 5), 3-phenylpyrazole derivatives (Patent Documents 6, 7, and 8), 2-phenyloxazole derivatives (Patent Document 9), and 2-phenylimidazole derivatives (Patent Document 9).
On the other hand, it is described that a compound represented by the following formula (II) has a uric acid-excreting action and is useful for therapy of hyperuricemia (Non-Patent Document 1). However, there are neither disclosure nor suggestion of the xanthine oxidase-inhibitory action and uric acid-synthesis inhibitory action in the document.

Moreover, it is suggested that a compound represented by the following general formula (III) is effective as antiinflammatory, antipyretic, analgesic, and diuretic agents (Patent Document 10).
wherein the groups COX and OY are ortho to each other and [Ar] is para to either COX or OY; [Ar] represents benzene or the like, R represents alkyl, halogen, alkoxy, cyano, nitro, or the like, a halogen atom, lower alkyl, or the like, X represents —OH, —NH2, alkylamino, or the like, Y represents a hydrogen atom, alkyl, alkenyl, aralkyl, or the like, and R1 represents a hydrogen atom or alkyl; see the publication for further information.
In addition, it is disclosed that a compound represented by the following formula (IV) has antiinflammatory and analgesic actions (Non-Patent Document 2).

However, in any of Patent Document 10 and Non-Patent Document 2, there are neither disclosure nor suggestion of the xanthine oxidase-inhibitory action and uric acid-synthesis inhibitory action.
Patent Document 1: WO92/09279
Patent Document 2: JP-A-2002-105067
Patent Document 3: WO96/31211
Patent Document 4: JP-A-57-85379
Patent Document 5: JP-A-6-211815
Patent Document 6: JP-A-59-95272
Patent Document 7: WO98/18765
Patent Document 8: JP-A-10-310578
Patent Document 9: JP-A-6-65210
Patent Document 10: DE2031230
Non-Patent Document 1: Annali di Chimica Applicata, Italy, 1931, Vol. 21, p. 553-558
Non-Patent Document 2: Journal of Medicinal Chemistry, USA, 1971, Vol. 14, p. 339-344